The major pumping chambers in the human heart are the left and right ventricles. The simultaneous physical contraction of the myocardial tissue in these chambers expels blood into the aorta and the pulmonary artery. Blood enters the ventricles from smaller antechambers called the left and right atria, which contract about 100 milliseconds (ms) before the ventricles. This interval is known as the atrioventricular (AV) delay. The physical contractions of the muscle tissue result from the depolarization of such tissue, which depolarization is induced by a wave of spontaneous electrical excitation which begins in the right atrium, spreads to the left atrium and then enters the AV node which delays its passage to the ventricles via the so-called bundle of His. The frequency of the waves of excitation is normally regulated metabolically by the sinus node. The atrial rate is thus referred to as the sinus rate or sinus rhythm of the heart.
Electrical signals corresponding to the depolarization of the myocardial muscle tissue appear in the patient's electrocardiogram. A brief, low-amplitude signal known as the P-wave accompanies atrial depolarization normally followed by a much larger amplitude signal, known as the QRS complex, with a predominant R-wave signifying ventricular depolarization. Repolarization prior to the next contraction is marked by a broad waveform in the electrocardiogram known as the T-wave.
A typical implanted cardiac pacer (or pacemaker) operates by supplying missing stimulation pulses through an electrode on a pacing lead in contact with the atrial or ventricular muscle tissue. The electrical stimulus independently initiates depolarization of the myocardial (atrial or ventricular) tissue resulting in the desired contraction. The P-wave or R-wave can be sensed through the same lead (i.e., the pacing lead) and used as a timing signal to synchronize or inhibit stimulation pulses in relation to spontaneous (natural or intrinsic) cardiac activity. The sensed P-wave or R-wave signals are referred to as an atrial electrogram or ventricular electrogram, respectively.
Modern-day implantable stimulation devices include cardiac event detecting/sensing circuitry, whether the activity of one or both chambers of the heart are sensed. A cardiac event is essentially detected when the sensed electrogram signal exceeds a defined sensitivity threshold level. If the sensitivity level is too low (e.g., the sensitivity threshold is set too high), then some intrinsic cardiac events may not be detected. If the sensitivity level is too high (e.g., the sensitivity threshold is set too low) then, on the other hand, the high gain of the amplifier may cause noise or T-wave signals to be sensed, giving rise to erroneous classifying of noise as a cardiac event. Devices provided with communications telemetry (e.g., noninvasive programming capabilities) advantageously allow the physician to manually set the sensitivity level.
There are at least two disadvantages to having the physician set the sensitivity level. First, adjusting the sensitivity level is one more thing that the physician must remember to do, and it would be advantageous to relieve him or her of that task if it is possible to do so. Secondly, and more important, the physician generally sees the patient only occasionally, and weeks or months may go by without the sensitivity level being changed. Problematically, the sensitivity level that will accurately detect cardiac events at a given threshold level for a patient does not stay static; e.g., the R-wave amplitude and frequency content can vary considerably within a given patient. Thus, changes in the sensitivity level are needed to accommodate for physical and mental stress. In addition, the sensitivity level needs to change as myocardial tissue (heart muscle tissue) undergoes scarring or other physical responses to the implanted electrogram lead(s). Furthermore, other changes in the myocardium-electrogram lead interface, e.g., shifting of the position of the electrogram lead, may also cause changes in the proper sensitivity level. There may also be a need to change the sensitivity due to internal and/or external electrical noise.
Unfortunately, many of these changes occur over a period of days and, in some cases, even hours or minutes. Because the physician generally sees the patient only every few weeks or months, the pacemaker sensing circuits can erroneously detect, or not detect, cardiac events over large periods of time. This erroneous detection/non-detection can cause under-pacing or over-pacing of the heart. Unfortunately for the patient, such changes may potentially leave him or her in a worse condition than he or she was in before the stimulation device was implanted. At best, the stimulation device is not able to operate efficiently—for example, by either unnecessarily providing therapy and thereby draining the battery and risking pacemaker-induced tachycardias; and/or not providing therapy as often as is needed by the patient.
Consequently, there is a need for improved methods and arrangements for dynamically adjusting the sensitivity of an implantable device to account for potential changes in the electrogram signal. Further, a need exists, as explained further below, for methods, devices, etc., that act to reduce risk of oversensing in implantable cardiac defibrillation devices (ICDs). Various exemplary methods, devices, systems, etc., presented herein aim to address these needs and/or other needs.